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Cardiology Dr Osama Mahmoud

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~Portal hypertensionr--.,...--:

Oes?hageal varices.

 

1-----+- Ascites,

 

2..l~enal~ein 1111·0111bosis

 

 

o Common in membranous

GN.

 

o Dehydration

 

 

o Blood disease C/P ELoin pain and tenderness.

 

worsening of kidney function?

3.. I"C tlU·Ol11bosis

Proteinuria.

 

 

 

 

Cause

0 Typhoid.

f} Behcet's

disease.

C/P

*

 

 

Edema of both lower limbs.

 

 

* Ascites.

 

 

 

* Collaterals on the abdominal

wall.

4.. S"C Th'·0111bosis

* Constrictive pericarditis. Mediastinal

 

Cause

mass.

 

*

 

*Facial edema.

*Congested non pulsating neck veins.

Chest collateralsdirected from above downward.

5..i~~illa,"i"ein Tlll·Oll1bosisC/P

CIP • Edema of the arm.

• Pain, tenderness along the course of axillary vein.

 

PULMONARY EMBOLI!iM

I

( Sources of pulmonary embolism:

1.DVT.

2.Infective endocarditis of right side of the heart.

3.Fat embolism. e.g bone fracture.

4.Amniotic fluid embolism.

S. Air embolism.

( C/P of pulmonary emboli: kAccording to the size of embolism)

~ C/p

J.~

S111a11 sized embolism

 

• No symptoms, but cough, dyspnea or chest discomfort may occur.

 

Recurrent embolization with obliteration of >2/3 of pulmonary vascular bed .

 

 

.

 

Thromboembolic pulmonary hypertension

Right

sided failure

(cor pulmotale) i.e. subacute cor pulmonale.

89

~ c/p:B- Moderatesized em.boli(Pujmonary

Cardi,,4ogy

Infarctfon)

 

1. Cough

 

 

 

2., Blood tinged sputum

 

 

3. Chest Pain

 

 

 

4. Dyspnea

5. Fever.

 

 

••••••••~IPaI •••

 

 

 

 

 

a -

Pleural

 

rub.

 

 

 

 

 

 

b- Crepitations

may present

over the involved area.

 

.

c-

Blood

 

stained effusion

may developed

(exudative

effusion) .

 

 

 

 

 

•••••••.•

.............................

 

.........

 

 

: The lung parenchyma has three sources of O2 i.e pulmonary vessels, bronchial

~vessels and air within alveoli so, the hemodynamics of the lung must be

~compromised for a lung infarction to occur on top of pulmonary embolism.

..................................•..........•....•............................................•..••....••.......

~Radiological Signs of Pulmonary Embolism

1.Normal X - ray.

2.Triangle (wedged shaped opacity) i.e pulmonary infarction.

3.Pulmonary oligemia = massive embolism.

4.Pleural effusion.

S.Pulmonary edema.

6.Dilated pulmonary artery.

~ Blood tests: l' TLC, l' ESR, t LDH,

> EC6

.,

Normal except for sinus tachycardia, AF may occur.

 

.,

Right ventricular strain may occur (inverted T in VI, V2)

 

.,

Right

axis deviation .

 

.,

Right

BBB.

~ Pulmonary angiography, it is diagnostic but invasive.

~ Lung scan:

I Ventilation Scan

Penusion

Scan

 

 

 

Patient

inspires (Xenon)

IV injection of radioactive

gas with radioactive material

material

(Tc)

We detect thedistribution

Lung uptake occurs

by pulmonary arteries,

of the

radioactive

this can be detected

by gamma camera

material by gamma camera

 

 

 

 

 

within

lung tissue, this 1i!!1% ~

'\1 This reflects

pulmonary

reflects

ventilation.

vascularity.

 

Normal ventilation scan + abnormal

perfusion scan highly suggestive for

pulmonary embolism.

 

 

 

In pulmonary fibrosis, there is abnormal ventilation scan with abnormal perfusion scan.

~ Spiral CT with IV contrast (CT pulmonary angiography).

90

lmonary embolism obstructing> 50 % of pulmonary

vasculature .

...•..-

 

 

 

 

1. Chest Pain

(similar to anginal pain) due to:

.

.

Hypotension

or shock (J.cop n

Hypoxia.

~

Angmal pam

Rapid distention of pulmonary artery.

2.Shock due to:

Marked decreased of blood flow to lung ~J.J. VR to left atrium

~J. COP ~ shock .

. 3. Cyanosis (hypoxia), tachypnea and tachycardia. 4. Acute right sided heart failure

Lower limb edema.

Enlarged tender liver.

• Congested neck veins, with prominent a wave.

S3 gallop on tricuspid area.

~Investigations

As above, blood gases showing hypoxia.

Treatment

of pulmonary

embolism & D.V.T

I. P,ophylactic

measures:

 

 

o Avoid prolonged post operative recumbency

specially in pelvic surgery (e.g

hysterectomy, hip surgery, prostatectomy).

 

@ In risky patients subjected to surgery

give:

 

mini dose heparin or low molecular

weight

heparin (post operative).

8 Treatment of the cause

118 aJiif14tfjtf.' iicfor massive embolism)

1.02 therapy.

2.Analgesics ~ Pethidine

3.Treatment of shock e.g with dobutamine, this will improve the right ventricular efficiency.

4.Treatment of cardiac arrest if occurs.

IIMTI·Ir!itlli1l1'!t".'''i·ar'l·III''.'~rt~tf''i~!tlla"4"f"i·'IlllJ"'~(for right ventricular failure and hemodynamic instability)

Streptokinase.

• Urokinase.

• Recombinant tissue plasminogen activator.

Value

~

Relief the obstruction of the pulmonary vasculature.

 

~

Improvement

of right ventricular efficiency.

 

~

Correction of the hemodynamic instability.

91

Card

Give 5000 - 10.000 units IV as a loading

dose.

Then 1000 units / hr IV infusion drip.

 

Heparin infusion is the best ~ Low

incidence of haemorrhage.

Why?

1.Maintained

therapeutic level all over

 

the day.

 

Other methods of heparin therapy:

 

'i 5000 - 7500 units

IV /6hrs

'i 10,000 units se / 8hrs.

 

Duration of heparin therapy ~

7-10 days or till clinical improvement.

Follow up by PTT is adjusted to be (l.5 - 2.5) of the control value Then start oral anticoagulant (Warfarin) for 3-6 months (as below).

IWarfarin

I

2.5-

7.5 mg/d.

 

 

 

 

 

 

 

 

The dose is adjusted according

to PT to be (1.5 - 2) of the control value

 

 

 

or to reach an INR value (2-3.5) according

to the need .

 

 

.•.•.•.....

••......

 

••........

•.....

••.....

. •••••. ....•••

.............

........

•......

•..........

•.•••.•

..

 

The insertion

of filter into Ive can be done if the anticoagulant

or

 

fibrinolytic

therapy

is contraindicated

or fails to inhibite

thromboembolism.

 

So high risk patients with contraindications

of anticoagulant

therapy

can be

 

treated by insertion

of a filter in the Ive above

the level of the renal

veins to .

••

 

 

 

 

prevent.embolisation,

••.•

 

•••.•.•..•••••

:

 

 

 

 

•.................

•..•......

~...

••

Pulmd~~jf~~bolism

 

should~.~ su~~~ctedin

patient with new onset-of

 

 

unexplainedqough,

dyspnea,

orhYJ?erventilation,

chest pain, haemoptysis,

 

AF, Of with

signs ..of P++ if no othy;t':cause can be found

 

 

 

 

 

92

DI§EA§E§ OF AORTA

I

( 1. Aneurysm of Ascend.ing Aorta )

~-tiQ1Q~~

'@ Syphilis (rare) '@ Cystic medial degeneration mainly in the eldery.

This is the aneurysm of signs. '@AI(see later).

'@ Dullness of aortic area. '@ Pressure 'on S.V.C.

'@ Pulsating aortic area.

(~2--.-A-n-e-u-ry-s-m--o-f-t-he--A-(Aneurysm-ch-) of symptoms) See chest (mediastinal $), it is usually due to atherosclerosis.

I 3. Dissecting Aortic AneUrysm]

~ Pathogenesis: Tear in the intima of aorta ~ Blood bursts into the media of the aorta (dissection) which is then split into two layers, the aortic valve may be damaged and the branches of the aorta may be compromised.

Wall of aorta

qJ q

I q

 

~:t~~~~~a~issects

~-~-

....- _---'7

~w~

 

/

 

through

the media

5ij I~

 

leading

to

 

 

narrowing of

branche

of aorta

the lumen with obstruction of branches of aorta at the site of dissection

~C/P: (Old male, hypertensive with chest pain)

¢Shock, 50% of patients may be hypertensive.

¢Severe chest pain (tearing) radiating to the back.

¢Obstruction of the opening of the branches from aorta ~ ischaemia. Occlusion of aortic branches may cause a variety of complications including myocardial infarction (coronary), paraplegia (spinal), mesenteric occlusion (caeliac), renal failure (renal) and acute limb ischaemia.

93

¢ Unequal pulse volume of both upper limbs or both lower limbs. ¢ Acute AI may occur due to widening of aortic root.

Types of dissecting

aortic aneurysm:

'i Type I

---+ Proximal

ascending aorta to descending.

'iType II ---+ Confined

to ascending aorta.

'i Type III --+ Descending aorta and distally.

~ Etiology:

1. Hypertension.

2. Atherosclerosis.

3. Collagen disease e.g. Marfan $ & Ehler Danlos $.

~D.D.: Acute chest pain + shock.

Extensive MI.

Massive pulmonary embolism.

Tension Pneumothorax.

Dissecting aortic aneurysm.

~Investigations:

¢CT scan is diagnostic.

¢MRI is highly accurate.

¢Chest X ray ---+broadening of mediastinum.

~Treatment:

• Control blood pressure specially with B- blockers to lessen shear forces.

• Surgery with replacing the affected part with a Dacron graft, aortic valve replacement may be needed.

Diseases of aorta:

Aortic aneurysm and its types.

Takayasu' s disease (Aortic arch $).

Coarctation of aorta.

Aortitis e.g in rheumatoid disease and sero negative arthropathy ---7 AI.

94

 

CO 1\1IiEI\I

IT AL HEART DI!iEA!iE

i

 

 

 

 

 

(0.8 % of live births)

 

 

 

•• \~hen ~Otl

stlsl,ect

congenital heart 'lisease?

 

 

 

1 -Age < 5 years.

 

 

 

 

2 - Hypertension

in a child.

 

 

 

 

3 -Positive prenatal history.

 

 

 

 

4 - Associated congenital anomalies.

 

 

 

 

5 -Cyanosis since birth.

 

 

 

 

6 - Negative

history of rheumatic fever.

 

 

 

 

7 - Thrill over the base (AS-PS) or left parasternal

(VSD)

 

C~IU e~\s~

'r:la c'"ifr!O\r.JS~l·\

 

 

 

~

-~~~

~=:I_=~:lSI=:I

~IJ

 

 

 

 

1- Genetic

abnormalities e.g congenital heart block, ASD.

 

 

2- Irradiation.

 

 

 

 

 

 

3- Maternal rubella (PDA, Pulmonary stenosis)

 

 

 

 

4- Premature

infants.

 

 

 

 

 

5- Chromosomal abnormalities e.g.: .:. Down's

syndromc-e-VSl) .

 

 

 

 

 

 

•:. Turner's

syndrome-scoarctation

of aorta

 

6- Maternal alcohol abuse (septal defects).

 

 

 

YI=:I_a

 

ri

 

 

 

 

Cll

~~~~e~s~ii*.Hiim'~1~SI=:I=(f)\D

 

 

 

 

• Cianotic

 

 

 

• A ",~anotic

l'olentialli

cStanotic

 

e Fallot's

tetralogy

e Coarctation of aorta.

e VSD.

 

 

e Fallot's

triology

e PSAS.

 

e PDA.

 

 

 

 

 

 

e Dextrocardia

 

e ASD.

 

Q':IThe commonest congenital heart diseases are bicuspid aortic valve and VSD. Q':IThe commonest con enital c anotic heart disease is Fallot's tetralogy

FALLOT'S TETRALOGY

It is the most common cyanotic anomaly in those who do survive and is commonest amongst adults.

~~~JOJllb~JllbtSJ .

Pulmonary stenosis (PS)

VSD.

Right ventricular hypertrophy.

Overriding aorta.

Pulmonary.

artery

95

Cardiotog9 "

1. P.s

f"'it'i~"th~'~~~t'i~p'~~t~~'t'i'~~i~~'th~t'd~t~~~i'~~~'th~"~~'~~~i

..........................................................................................................................................

~It is infundibular = subvalvular due to abnormal tissue deposition, (right ventricular outflow obstruction).

~

The sub valvular tissue

is supplied

by adrenergic receptors,

so, the

 

RV outflow

obstruction

is dynamic

and may increase suddenly

under

 

adrenergic

stimulation.

 

 

 

~

PS is the most important lesion as it determines the amount of blood

 

ejected to the lung.

 

 

 

 

 

lSevereR.S .il

I

 

 

I MildPS .

 

 

• Decreased

blood flow to the lung .

 

 

• Increased

blood flow to the aorta.

 

 

 

 

!

 

(jj= Mild Cyanosis.

 

 

(jj= Severe cyanosis.

 

Cyanotic spells (Fallot's spells)

Exertion ~ isympathetic discharge with adrenergic stimulation of the subvavlular tissue ~ spasm of the infundibulum ~.1PS ~ i blood..flo\Vto the aorta

~ severe cyanosis & hypoxia ~ hypQxic syncope·Ccyanotic spells)

4~.aL~Q)Bt

O2 therapy .

 

 

 

 

 

 

Beta blocker IV or diamorphine

to relax the right

 

 

 

 

ventricular outflow

obstruction .

 

 

2. V.S.D.

Squatting position.

 

 

 

 

 

 

 

 

 

 

It is silent (no murmur)

why?:

 

 

• As it is a wide VSD .

 

 

 

Both ventricles are

 

.ected to the same aortic pressure !?

 

••

This leading

to central cyanosis.

 

 

 

01 ;fttlttl't,,;

lafA

 

i i61a;\il~1"I;t.] ~,;,,~

 

 

••

It is mild ~

because

 

it has 2 pathways:

0 Pulmonary

artery.

f} Aorta.

CfmJ CD Cyanosis

since birth or when the

@ Secondary

 

 

ductus closes, the time of it's closure

polycythemia

 

 

is very variable i.e it may close late,

usually

present.

 

 

even after one year.

 

 

 

 

@ Clubbing

of fingers.

 

@ Squatting position

 

@ Stunted

growth

 

 

 

Acianotic l~allot'stetralod

(pink tetral;;> .. .. "

 

(Mild PS)

 

It is presented

~

 

with exertional cyanosis.

~As

exertion

--+ decreaseP-R :;::>

Infundibular spasm

IIblood flow to aorta.

~

Decrease blood flow to the lung.

Inspection

Palpation

Percussion

Auscultation

1. Murmur

murmur over

Pulmonary

component

pulmonary area.

 

High pressure due to aortic over blood flow ~ Loud aortic component.

Low pulmonary

pressure ~ J-l-pulmonary

component

l

N

00.

-"0e=

Thrill may be palpable in the second left space close to the sternum.

1.

X-ray

Coeur

en sabot heart (Rt Y++)

2.

ECG

Right

ventricular

hypertrophy.

3.

Echocardiography

 

 

 

 

4.

Catheter

Measures

pressure-ohigh

right ventricular pressure.

 

 

• Measures

O2 ~

Low O2

of aorta.

Passes through anomaly (through YSD)

Injection of dye ~ reveal the abnormality .:

97

Cardiology

(A)Medical: Treatment of Fallot's spells and prophylaxis for endocarditis.

(B)Surgical:

It is a palliative procedure called

Innominante

artery

Shunt between left subclavian

and left pulmonary artery

Right ~

Right common carotid

 

VAlUE:

 

 

 

= Improvement

of cyanosis and general condition.

 

= Improvement

of the vasculature of the attenuated

pulmonary vessels.

=Sometimes it is done in cases of too hypoplastic pulmonary arteries without total correction specially in later life.

(the Best)

Complete surgical correction is possible even in infancy, before the occurance of hypoplasia of pulmonary arterioles.

 

[F-TRIOLOGY )

[F-TETRALOGY )

._---

ASH +PS +Huge RT.

'i Mild RtV+ +.

 

'i Huge right V.

Neck veins is not congested.

 

'i<Congestedneckveins.

Cyanosis Since birth.

 

'iCyanosis is delayed

Single loud S2

 

'i S2 is weak with

 

 

wide splitting

 

 

 

Huge"Rt.V

L

* The reversed

shunt

cyanosis,

this is not

Eisenmenger's

synd1;ptr1e

 

 

because

there is no·P+·+

 

F. Pentalogy

(F4+ASD).

 

 

98

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